EGFR-Dependent Regulation of Matrix-Independent Epithelial Cell Survival. Addendum
Final addendum rept. 15 Mar 2006-14 Mar 2007
THOMAS JEFFERSON UNIV PHILADELPHIA PA
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Signaling through the epidermal growth factor EGFR has been implicated in both effective wound healing and epithelial neoplasia. We have identified a novel function of the EGFR in support of epithelial cell survival, particularly in conditions of anchorage-independence. ObjectiveHypothesis Define molecular mechanisms and pathways by which EGFR activation supports epithelial cell survival. Two specific aims focus on 1 posttranslational modification of relevant Bcl-2 family members by EGFR activation through MAPK-dependent mechanisms and, 2 STAT3 activation by deregulated EGFR signaling as observed in epithelial cancer. Work related to Specific Aim 1 has been completed and published in three manuscripts during 2006. In addition, another manuscript has been accepted for publication in 2007. The final action item, i.e. assessment of JNK and p38 activation in the anchorage-independent state as they relate to NF-kappaB activity has been completed. In summary, we have completed the work proposed in both, Specific Aims 1 and 2 of the original proposal.
- Anatomy and Physiology
- Medicine and Medical Research